PRMT6 (Protein Arginine Methyltransferase 6)

This study provides evidence that hypoxia mediates TMZ resistance in GBM through the HIF-1α/PRMT6/G3BP1 axis, identifying PRMT6 and G3BP1 as promising therapeutic targets to overcome chemoresistance.

Epigenetic modification may be a mechanism linking social exposure and biological changes. Addressing neighborhood-level social stress exposure may improve the prevention and intervention of lung cancer.

Exposure to social stress may contribute to higher levels of PRMT6. Social and biological differences affecting race and sex groups need further investigation.

In addition, dual-luciferase experiments showed that the transcription factor KLF4 may bind to the -1800 ~ +45 sequence of PRMT6, thereby negatively regulating PRMT6 expression in melanoma. Our findings underscore the tumor-suppressive role of PRMT6 in melanoma pathogenesis, highlighting its potential as a novel therapeutic target, particularly for metastatic melanoma.

Inhibiting PRMT6 with MS023 or mutating the RBM39 methylation site enhances Indisulam sensitivity in NSCLC and significantly improves its anti-tumor efficacy. Our findings identify methylated RBM39 as a key biomarker of Indisulam resistance and suggest a potential therapeutic strategy for NSCLC.

We measured L-arginine and its metabolites L-ornithine, L-citrulline, ADMA, and SDMA in a prospective cohort of 243 women with primary breast cancer (BC) and their associations with mortality and disease recurrence during 88 (IQR, 82-93) months of follow-up...ADMA is a prognostic biomarker in Luminal A patients; its metabolizing enzyme, DDAH, is highly overexpressed in BC cells. Thus, fingerprinting of L-arginine metabolism may offer novel personalized treatment options within BC subtypes.

Our study provides a preclinical proof of concept to overcome resistance to immunotherapy by targeting PRMT6 in CRC with MSS.

By treating human lymphoma cells, we found that PCL-TPE@1 was able to effectively reduce the migratory ability of lymphoma cells by inhibiting the expression of PRMT6. This platform is easy to synthesize, offers thermo-responsive fluorescence, flexibility, and biocompatibility, making it suitable for biomedical drug delivery and smart devices.

Additionally, protein arginine methyltransferase-6-mediated modulation of heterogeneous nuclear ribonucleoprotein-F expression required amino acids 319 to 388, but not classical H3R2 methylation. These findings indicated that protein arginine methyltransferase-6 is a potential therapeutic target for the treatment of peripheral neuropathic pain.

Our findings illustrate that PRMT6 suppresses TRAF6 transcription via H3R2me2a to enhance the protein stability of EZH2 to facilitate glioblastoma cell invasion and migration. Blocking the PRMT6-TRAF6-EZH2 axis is a promising strategy for inhibiting glioblastoma cell invasion and migration.

PRMT6-mediated protein stability inhibits the infiltration of CD8+ T cells, resulting in immune evasion of gastric cancer. The PRMT6-ANXA1 may be a promising strategy for gastric cancer.

Our results demonstrate the PRMT6-YTHDF2-Wnt-β-Catenin axis promotes GBM migration, invasion, and EMT in vitro and in vivo, potentially serving as a therapeutic target for GBM.